SIRT1‐mediated amelioration of oxidative stress in kidney of alcohol‐aflatoxin‐B1‐induced hepatocellular carcinoma by resveratrol is catalase dependent and GPx independent

2020 ◽  
Vol 34 (11) ◽  
Author(s):  
Divya Rawat ◽  
Somi Shrivastava ◽  
Rayees Ahmad Naik ◽  
Saurabh Kumar Chhonker ◽  
Raj Kumar Koiri
2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Brajesh Kumar Maurya ◽  
Surendra Kumar Trigun

Fisetin, a known antioxidant, has been found to be cytotoxic against certain cell lines. However, the mechanism by which it inhibits tumor growthin vivoremains unexplored. Recently, we have demonstrated that Aflatoxin-B1 (AFB1) induced hepatocarcinogenesis is associated with activation of oxidative stress-inflammatory pathway in rat liver. The present paper describes the effect ofin vivotreatment with 20 mg/kg b.w. Fisetin on antioxidant enzymesvis-a-visoxidative stress level and on the profile of certain proinflammatory cytokines in the hepatocellular carcinoma (HCC) induced by two doses of 1 mg/kg b.w. AFB1 i.p. in rats. The reduced levels of most of the antioxidant enzymes, coinciding with the enhanced level of reactive oxygen species in the HCC liver, were observed to regain their normal profiles due to Fisetin treatment. Also, Fisetin treatment could normalize the enhanced expression of TNFαand IL1α, the two proinflammatory cytokines, reported to be involved in HCC pathogenesis. These observations were consistent with the regression of neoplastic lesion and declined GST-pi (placental type glutathione-S-transferase) level, a HCC marker, in the liver of the Fisetin treated HCC rats. The findings suggest that Fisetin attenuates oxidative stress-inflammatory pathway of AFB1 induced hepatocarcinogenesis.


2020 ◽  
Vol 17 (3) ◽  
pp. 191-199
Author(s):  
Seval Yilmaz ◽  
Fatih Mehmet Kandemir ◽  
Emre Kaya ◽  
Mustafa Ozkaraca

Objective: This study aimed to detect hepatic oxidative damage caused by aflatoxin B1 (AFB1), as well as to examine how propolis protects against hepatotoxic effects of AFB1. Method: Rats were split into four groups as control group, AFB1 group, propolis group, AFB1+ propolis group. Results: There was significant increase in malondialdehyde (MDA) level and tumor suppressor protein (TP53) gene expression, Glutathione (GSH) level, Catalase (CAT) activity, CAT gene expression decreased in AFB1 group in blood. MDA level and Glutathione-S-Transferase (GST) activity, GST and TP53 gene expressions increased in AFB1 group, whereas GSH level and CAT activity alongside CAT gene expression decreased in liver. AFB1+propolis group showed significant decrease in MDA level, GST activity, TP53 and GST gene expressions, GSH level and CAT activity and CAT gene expression increased in liver compared to AFB1 group. Conclusion: These results suggest that propolis may potentially be natural agent that prevents AFB1- induced oxidative stress and hepatotoxicity.


2021 ◽  
Vol 225 ◽  
pp. 112754
Author(s):  
Qin-qin Cao ◽  
Lu-xi Lin ◽  
Ting-ting Xu ◽  
Ying Lu ◽  
Chao-dong Zhang ◽  
...  

Hepatology ◽  
1992 ◽  
Vol 16 (5) ◽  
pp. 1150-1155 ◽  
Author(s):  
Chien-Jen Chen ◽  
Yu-Jing Zhang ◽  
Sheng-Nan Lu ◽  
Regina M. Santella

Oncogene ◽  
2021 ◽  
Author(s):  
Shouping Wang ◽  
Kun Cao ◽  
Yuting Liao ◽  
Wei Zhang ◽  
Jihua Zheng ◽  
...  

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